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In Vitro Modeling of Extracellular Trap Release and Association with LL‐37 Peptide in THP‐1‐Derived Macrophages
Author(s) -
Stone Sophia,
Craig Maria
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.571.7
Subject(s) - neutrophil extracellular traps , antimicrobial peptides , innate immune system , phagocytosis , microbiology and biotechnology , biology , extracellular , immune system , monocyte , peptide , macrophage , in vitro , chemistry , inflammation , biochemistry , immunology
Leukocyte‐derived extracellular traps (ETs) are DNA webs coated with histones and antimicrobial peptides that ensnare and kill bacteria in a phagocytosis‐independent manner. The cell death pathway resulting in ET release (ETosis) has been studied extensively in neutrophils, but it is now known to occur in other immune cell types via similar mechanisms. Antimicrobial peptide LL‐37 is a potent DNA‐binding peptide that facilitates ETosis in neutrophils and protects neutrophil ETs (NETs) from degradation by bacterial nucleases. Here, quantification of extracellular DNA was performed using immunocytochemistry and fluorimetric analysis to study immunogenic species that may activate ETosis in THP‐1 monocyte‐derived macrophages. We will also investigate a potential role for LL‐37 in the formation and antimicrobial activity of monocyte/macrophage ETs (METs). Shared ETotic mechanisms exist between multiple leukocyte lineages, but cooperative targeting of diverse microbial species via specialized mechanisms could contribute to broad‐spectrum innate immune defense, as well as inflammatory tissue damage in human diseases. This work was supported by a grant from the TriBeta Research Scholarship Foundation.